ArticleJCI insight2017
Increased Ca2+ signaling through CaV1.2 promotes bone formation and prevents estrogen deficiency-induced bone loss.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Electric field stimulation-responsive hydrogels for bone regeneration: from mechanisms to applications.Bone research · 2026Review
- Exploring Metabolic Mechanisms in Calcific Tendinopathy and Shoulder Arthrofibrosis: Insights and Therapeutic Implications.Journal of clinical medicine · 2024Review
- Multiple beta cell-independent mechanisms drive hypoglycemia in Timothy syndrome.Nature communications · 2024Article
- An L-type calcium channel blocker nimodipine exerts anti-fibrotic effects by attenuating TGF-β1 induced calcium response in an in vitro model of thyroid eye disease.Eye and vision (London, England) · 2024Article
- The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging.Aging and disease · 2024Review
- Loss of the auxiliary αJBMR plus · 2024Article
- The role of calcium channels in osteoporosis and their therapeutic potential.Frontiers in endocrinology · 2024Review
- Fibrillin-1 mutation contributes to Marfan syndrome by inhibiting Cav1.2-mediated cell proliferation in vascular smooth muscle cells.Channels (Austin, Tex.) · 2023Article
- Convergence of Calcium Channel Regulation and Mechanotransduction in Skeletal Regenerative Biomaterial Design.Advanced healthcare materials · 2023Review
- Examining Mechanisms for Voltage-Sensitive Calcium Channel-Mediated Secretion Events in Bone Cells.Calcified tissue international · 2023Review
- The intricate mechanism of PLS3 in bone homeostasis and disease.Frontiers in endocrinology · 2023Review
- Low-intensity pulsed ultrasound/nanomechanical force generators enhance osteogenesis of BMSCs through microfilaments and TRPM7.Journal of nanobiotechnology · 2022Article
- Calcium released by osteoclastic resorption stimulates autocrine/paracrine activities in local osteogenic cells to promote coupled bone formation.American journal of physiology. Cell physiology · 2022Article
- Increased Ca2+ influx through CaV1.2 drives aortic valve calcification.JCI insight · 2022Article
- The role of TRPV channels in osteoporosis.Molecular biology reports · 2022Review
- Genetic variations for the eggshell crystal structure revealed by genome-wide association study in chickens.BMC genomics · 2021Article
- STING suppresses bone cancer pain via immune and neuronal modulation.Nature communications · 2021Article
- Comparative Proteomic and Metabolomic Analysis of Human Osteoblasts, Differentiated from Dental Pulp Stem Cells, Hinted Crucial Signaling Pathways Promoting Osteogenesis.International journal of molecular sciences · 2021Article
- Skeletal Functions of Voltage Sensitive Calcium Channels.Current osteoporosis reports · 2021Review
- Voltage-Gated Calcium Channels in Nonexcitable Tissues.Annual review of physiology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
While the prevalence of osteoporosis is growing rapidly with population aging, therapeutic options remain limited. Here, we identify potentially novel roles for CaV1.2 L-type voltage-gated Ca2+ channels in osteogenesis and exploit a transgenic gain-of-function mutant CaV1.2 to stem bone loss in ovariectomized female mice. We show that endogenous CaV1.2 is expressed in developing bone within proliferating chondrocytes and osteoblasts. Using primary BM stromal cell (BMSC) cultures, we found that Ca2+ influx through CaV1.2 activates osteogenic transcriptional programs and promotes mineralization. We used Prx1-, Col2a1-, or Col1a1-Cre drivers to express an inactivation-deficient CaV1.2 mutant in chondrogenic and/or osteogenic precursors in vivo and found that the resulting increased Ca2+ influx markedly thickened bone not only by promoting osteogenesis, but also by inhibiting osteoclast activity through increased osteoprotegerin secretion from osteoblasts. Activating the CaV1.2 mutant in osteoblasts at the time of ovariectomy stemmed bone loss. Together, these data highlight roles for CaV1.2 in bone and demonstrate the potential dual anabolic and anticatabolic therapeutic actions of tissue-specific CaV1.2 activation in osteoblasts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.